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Med School > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is OA?
Symptoms?

A
  • wearing out of hyaline articular cartilage of diarthrodial joints
  • considered non-inflammatory, most common cause of chronic arthritis
  • joint pain, inactivity stiffness, decreased ROM
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2
Q

Causes leading to OA

A
  • age
  • injury
  • obesity
  • chronic inflammation of joint
  • Paget’s (abnormal stiff subchondral bone)
  • Avascular necrosis (abnormal weak subchondral bone)
  • in hip specifically - shallow acetabulum, femoral head tilt, femoral acetabular impingement
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3
Q

Where is OA common?

A
  • large weight-bearing joints like hips/knees
  • knee OA is most common
  • can also be in the hands (DIPs, PIPs)
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4
Q

Effect of OA on knees

A
  • Varus deformity of the knees
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5
Q

Diarthrodial Joints

A
  • mobile, peripheral
  • hyaline articular cartilage made of type 2 collagen and aggregated proteoglycans
  • surrounded by fibrous capsule lined by synovium
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6
Q

Describe articular cartilage - main cell present?

A
  • chondrocytes are the only cells present - no blood or nerve supply, nutrients come from the synovial fluid
  • chondrocytes produce both type II collagen and PGs
  • # of chondrocytes is fixed once you reach adulthood
  • does not regenerate once it wears out
  • radiolucent (black/grey) on x-ray - not calcified
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7
Q

What happens at a cellular level in OA?

A
  • chondrocytes multiply in lacunae to try and synthesize more matrix
  • however, this cannot keep up with the up-regulation of matrix metalloproteases
  • less PG aggregates due to cleaving at hook region by aggrecanase
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8
Q

Describe the matrix of articular cartilage

A
  • 90% water - hydrophilia of PGs allows for compliance, deformability, shock absorption
  • type II collagen - arranged in branch arches, helps prevent breakdown of PGs, tensile strength, impact loading
  • proteoglycans - (-) charged combinations of protein and sugar
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9
Q

Describe the structure of a proteoglycan

A
  • bottle brush configuration
  • central core protein with GAGs attached (- charged and thus attract water)
  • hook region near amino terminal (aka hyaluronic acid binding region) which allows multiple PGs (aggrecans) to attach to HA
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10
Q

What are the two different GAG types?

A
  • chondroitin sulfate - larger, located superiorly (carboxyl end), mostly galactosamine disaccharides
  • some revision from C-6s (adult) to C-4s (fetal) in OA
  • keratin sulfate - shorter, located proximally (amino end), enriched in glucosamine

*core protein has a unique a.a. sequence that determines where these GAGs attach

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11
Q

What is happening in the knee joint during compression/ relaxation?

A
  • compression - water released by PGs into synovial space
  • relaxation - water reimbibed into cartilage
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12
Q

What are the different neutral matrix metalloproteases? What makes them?

A
  • collagenase 1 (MMP 1) - targets type II collagen
  • stromelysin (MMP 3) - targets PGs
  • collagenase 13 (MMP 13) - targets type II collagen

*all made by chondrocytes

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13
Q

What up regulates MMPs?
What inhibits them?

A
  • IL-1 (made by chondrocytes, which have an IL-1 receptor), plasmin
  • normally TIMPs block MMPs, but in OA MMPs overwhelm
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14
Q

What happens in OA with regard to:
- water content
- PG aggregates
- collagen
- metachromatic stain
- surface
- chondrocyte number
- MMP enzymes
- subchondral bone
- osteophytes

A
  • Initially there is swelling due to water influx, then water loss and the joint becomes dry
  • PGs and collagen decrease
  • There is decreased uptake in metachromatic staining
  • Bone surface becomes irregular and fibrillated
  • Chondrocyte # increases due to mitoses in brood capsules
  • MMP enzymes increase
  • Subchondral bone comes sclerotic and there is presence of osteophytes
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15
Q

inflammatory mechanisms in OA

A

synovitis, IL-1, crystals

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16
Q

Primary vs Secondary OA

A

primary - localized, generalized such as in hands

secondary - chronic inflammatory arthritis (RA), identifiable mechanical/ congenital/ metabolic factors (i.e. hemochromatosis)

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17
Q

Names of enlargements at DIPs and PIPs

A

DIPs - Heberden’s nodes
PIPs - Bouchard’s nodes

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18
Q

Examples of inflammatory back pain
- common sx

A
  • ankylosing spondylitis, sero (-) spondyloarthropathy
  • under 40, prolonged morning stiffness, better with activity and worse with rest, nocturnal awakening, alternating buttock pain
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19
Q

Examples of infiltrative back pain

A
  • malignancy (primary or metastatic from breast/lung/ prostate)
  • infections (discitis, osteomyelitis, epidural abscess, TB)
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20
Q

What are back pain red flags?
(really only need blood work or imaging if these are present)

A
  • pain at rest or at night
  • history of trauma
  • history of malignancy
  • B symptoms (fever, weight loss, night sweats)
  • incontinence
  • saddle anesthesia
  • substance use disorder
  • steroids or immunocompromised
  • first episode after the age of 50
  • decreased passive range of motion
  • midline tenderness
  • new or progressive neuro issue (spasticity)
  • loss of balance, abnormal gait
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21
Q

Cauda Equina Syndrome
- sx
- dx
- tx

A
  • occurs when end of the spinal cord (L4-S4) is compressed (tumor, disc, infection, metastases)
  • acute or chronic back pain, saddle anesthesia (S3-5), bladder and bowel dysfunction (S2-3), lower leg weakness/ sensory changes
  • Dx: CT or MRI
  • Tx: emergency! surgical decompression
22
Q

Discogenic Back Pain

A
  • often a normal asymptomatic part of aging, do NOT treat imaging findings if no pain or symptoms
  • however, can be DDD or a herniation
23
Q

Degenerative Disc Disease (DDD)

A
  • micro fracture of collagen and loss of PGs leading to a desiccated disc
  • see disc space narrowing on X-ray
  • chronic onset
24
Q

Disc Herniation
- imaging
- sx

A
  • often acute due to lifting/ specific injury
  • best seen on CT/MRI
  • weakness, dermatomic pain, reflex loss, can be lateralized or central
25
Q

Facet Arthropathy
- sx
- imaging

A
  • facet joints (aka zygaphyseal joints) are synovial with hyaline surface, thus prone to OA
  • most commonly due to aging
  • unilateral neck/ lower back pain in non-dermatomic pattern
  • pain worse with leaning back/ lumbar extension/ lateral flexion
  • CT/MRI most useful, bone scan can demonstrate increased uptake suggesting active bone turnover and pain
26
Q

Spondylolithesis
- sx

A
  • one vertebra is sitting forward on the one below it
  • non-union, lysis, fracture
  • often developmental variation of neural arches (spondylolysis)
  • worse pain with forward flexion
27
Q

Spinal Stenosis
- sx for both spinal and vascular
- dx

A
  • narrowing of the spinal canal
  • can be congenital, osteophytes from facet hypertrophy, central disc herniation, mass effect from tumor or abscess, ligaments flavour hypertrophy
  • if spinal claudication - worse with walking, spinal claudication worse with walking, better with sitting, better with bending forward, walking uphill is easier
  • if vascular claudication - worse with walking, better with stop and stand, risk factors for PVD/ artherosclerosis, abnormal ABI, weak pedal pulses
  • Dx: CT or MRI
28
Q

Neural Foraminal Stenosis

A
  • facet joints narrow due to osteophytes
  • leaning to the affected side increases pain
29
Q

SI Ligament Sprain
- sx
- causes

A
  • buttock pain, difficulty sitting or standing
  • acute injury, overuse, muscle weakness, imbalance
30
Q

Scoliosis
- sx

A
  • sideways curvature of the spine
  • mild or asymptomatic, if severe can cause pain and respiratory issues
  • often genetic and will develop overtime in chidlhood
31
Q

In summary, which back pain syndromes are worse with flexion and which are worse with extension?

A

worse with flexion - spondylolitheis, discogenic pain

worse with extension - facet arthropathy, spinal stenosis

32
Q

Role of PTs and OTs in OA?

A

PT - self management, therapeutic exercise, PA guidelines, manual therapy

OT - joint protection (splints, orthoses, footwear), energy conservation, ADLs

33
Q

What is general non-surgical/pharmacological treatment for OA/ back pain?

A

EVIDENCE BASED: education, self-management, exercise (esp. quad strengthening), weight loss (dose-response relationship)

  • avoid bed rest
  • canes (NOT poles) are recommended for knee and hip OA (use opposite from affected side, wrist crease level when standing in shoes)
  • neuromuscular training, aerobic exercise, flexibility
  • potentially orthotics i.e. knee unloader brace/ braces/ laser/ TENS/ acupuncture, etc.
34
Q

What role do adipocytes have in OA?

A
  • release leptons and adiponectins that can lead to joint damage directly
35
Q

Oral treatments for OA

A

Acetaminophen - can push to 3-4g/day if normal kidney and liver function

NSAIDs - helps with inflammation and pain

Opiates - i.e. tramadol, tramacet… controversial, can try Tylenol T3s or start with tramadol

Duloxetine (SNRI) - moderate evidence for knee OA

Alternatives - ginger, apple cider vinegar, CBD oil

36
Q

Cons of NSAIDs (non-selective and selective)

A

non-selective - gastropathy especially if over 55
- use PPI for protection

  • COX-2 selective (celecoxib) - no effect on upper GI mucosa

Both - affect renal function, increase BP, CV risks, lower GI upset (do NOT give if IBD)
- if on them chronically, need to monitor liver and creatinine/ CBC

37
Q

Topical anti-inflammatories or analgesics for OA

A
  • diclofenac (voltaren) - some efficacy, 1st line
  • capsaicin - less evidence, more for neuropathic pain
38
Q

Injections

A
  • injectable corticosteroids - i.e. kenalog, Depomedrol
  • no more than 3 injections in one joint EVER, no more than 2-3 per year
  • inhibit IL-1 and MMPs, decrease inflammation
  • viscosupplementation/HA - not recommended, unclear efficacy, still widely done
  • platelet rich plasma (PRP) - centrifuged platelets, GFs, and cytokines re-injected
  • does NOT regenerate cartilage, no current evidence
39
Q

Glycosamine Sulfate (GLS-500) and Chondroitin Sulfate

A
  • provide GAG substrate
  • inhibit IL-1 and MMPs
  • however, no proven role yet
40
Q

DMOADs

A
  • disease modifying anti-OA drugs
  • some efficacy seen in strontium and tetracycline - inhibit MMPs
41
Q

Possible future treatments in OA

A
  • cartilage/ chondrocyte transplants
  • growth peptide
  • TIMPs (tissue inhibitors of metalloproteases)
  • mesenchymal stem cells, bone marrow aspirate concentrate
42
Q

What are some tools used to assess outcomes in OA?

A
  • WOMAC and AIMS2
43
Q

OA history taking

A
  • always ask about arthritis or psoriasis
44
Q

What is an acute onset of joint pain likely to be?

A
  • infection (septic arthritis) i.e MRSA, will see r-sided endocarditis
  • trauma
  • gout or pseudogout
  • renters disease
45
Q

Gout

A
  • acute onset, older age, diuretics, beer, rich food, past history
  • can get in the knee, but big toe most common
  • will likely see high serum uric acid, check fasting lipids as often metabolic
  • arthrocentesis (joint aspiration) - look for infection/ crystals (yellow parallel, negatively bi-refringent)
46
Q

Pseudogout

A
  • often caused by calcium pyrophosphate dehydrate crystals (CCPD)
  • will see chonedrocalcinosis on xray
  • blue parallel, yellow perpendicular crystals
47
Q

Indications for surgery in OA

A
  1. Nonoperative management has been maximized
  2. Pain interfering with QoL
  3. Reasonable expectations of joint replacement from the patient
  4. Pathology resulting in adult arthritis

Knee - medial OA, over 60, correctable deformity, stable knee

48
Q

Surgical treatment for Hip OA

A
  • total hip arthroplasty - very successful, replacements last 30+ years
49
Q

Surgical treatment for knee OA
- arthroscopic debridement
- arthroscopic microfracture
- autologous cartilage implantation
- allograft osteochondral transplant
- high tibial osteotomy
- knee arthroplasty

A
  • arthroscopic debridement - not common but maybe if unstable meniscus
  • arthroscopic microfracture - creating small fractures to stimulate bone marrow cells for cartilage regeneration
  • best for small symptomatic lesions under 2cm
  • requires careful rehab, mod improvement, but inconsistent results
  • autologous cartilage implantation - great results
  • take several cylindrical plugs from non-weight bearing zone to deficient area
  • allograft osteochondral transplant - harvested from cadaver (needs immediate transplant)
  • high tibial osteotomy - consider if medial compartment is arthritic and nothing else
  • offloads the medial compartment by realigning the tibia
  • good for young active patients with moderate arthritis in the medial compartment
  • knee arthroplasty - partial or total, replaces entire tibiofemroal joint and patella
  • not as good as total hip replacement
  • meant to treat pain, NOT to restore athleticism
50
Q

Contraindications for surgery in OA

A
  • panarthroses
  • young
  • obese
  • labourer
  • varus over 10
  • ACL deficiency
  • crystalline/inflammatory arthropathy

Med School (21 decks)

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